Indigofera tinctoria Linn. (Family Leguminosae, Hindi-Neel) is an annual herbaceous shrub, 4–6 ft. high, found throughout India. Earlier it was cultivated in India, China and other eastern countries as a source of Indigo.
In an indigenous system of medicine, extract of this plant is used for the treatment of epilepsy, nervous disorders and bronchitis [Wealth of India, vol. 5 (Council of Scientific and Industrial Research, New Delhi) 182, (1959)]. The plant is also known to be used as an ointment for sores, old ulcers and haemorrhoids [R. N. Chopra, S. L. Nayar and I C Chopra, Glossary of Indian Medicinal Plants, 141 (1956)]. The leaves of the plant have been used in liver ailments [Nadkarni, K. M., Indian Materia Medica, vol. 1 (Popular Book Depot, Bombay, 680 (1954)].
Organic solvent extract of the leaves of the plant exhibited marked hepatoprotective effect against carbon tetrachloride induced hepatic injury in rabbits, rats and mice [Anand, K. K., Chand Dewan, Ghatak, B. J. Ray & Arya, R. K., Indian J. Expl. Biol. 19, 298 (1981), Anand, K. K., Chand Dewan & Ghatak, B. J. Ray, Indian J. Expl. Biol., 17, 685(1979)].
Literature survey revealed that earlier reports showed the presence of trans-tetracos-15-enoic acid in Jojoba oil ex. Simmondsia chinensis seeds (0.62–1.11%), c/s isomer of the acid in fatty acids of the seed oil of. Microula sikkimensis (1.2%). [Wang, Huiying, Yu, Xuefian, Yi, Yuanfen & Ding, Jingkai, Yunnan Zhiwu Yanjiu 1989 11 (I), 60-4 (Ch.), L, Jing Jingmin; Wang, Jingping; Yu, Feuglau. Zhiwn, Xuebao, 1989, 31 (1) 50-3; (Ch). These reports do not mention isolation of the constituent and the content estimation is based on GLC data.
The bioactive constituent thus isolated in the present invention from the plant Indigofera tinctoria is designated as RLJ-NE-598 (025)(F)(A3) (TCA)
Hepatotoxins that cause acute hepatitis have close resemblance with the viral hepatitis-clinically, biochemically and histologically. Drugs also cause of chronic hepatic disease as chronic hepatitis, fatty liver, cirrhosis and several vascular lesions of the liver.
In many instances drug induced hepatitis proves indistinguishable from viral hepatitis. Chemically induced hepatic injury for experimental studies should be severe enough to cause cell death or to modify hepatic functions. The mechanism of acute hepatic injury depends upon the chemical compound and the species of animals used. Many chemicals produce parenchymal damage, arrest bile flow and cause jaundice (choleretic injury).
In the present invention the applicants have studied hepatoprotective activity against CCl4, paracetamol (APAP, acetaminophen), D-galactosamine and alcohol induced hepatotoxicity.